Expression of p-p38MAPK, uPA and Ki-67 in epithelial odontogenic tumour
10.3760/cma.j.issn.1002-0098.2010.09.006
- VernacularTitle:磷酸化p38促分裂原活化的蛋白激酶、尿激酶型纤溶酶原激活物及Ki-67在牙源性上皮性肿瘤中的表达
- Author:
Yi ZHONG
1
;
Li WANG
;
Xin-Ming CHEN
Author Information
1. 武汉大学口腔医学院
- Keywords:
p38 mitogen-activated protein kinases;
Urinary plasminogen activator;
Ki-67 antigen;
Epithelial odontogenic tumour
- From:
Chinese Journal of Stomatology
2010;45(9):535-539
- CountryChina
- Language:Chinese
-
Abstract:
Objective To examine the expression of phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK) , urokinase plasminogen activator (uPA) and Ki-67. Methods The specimens of ameloblastoma (AB) , keratocystic odontogenic tumour (KCOT) , calcifying epithelial odontogenic tumor (CEOT), adenomatoid odontogenic tumour (AOT) , calcifying cystic odontogenic tumour (CCOT) and 5 tooth germs were examined immunohistochemically for the expression of p-p38MAPK, uPA and Ki-67. Results p-p38MAPK was detected both in the cytoplasm and the nucleus of the epithelial odontogenic tumour cells and uPA in the cytoplasm of the epithelial odontogenic tumour cells. Among the 65 cases, there were 17(26%) ,51 (78%) and 62 cases(95%) of positive expression of p-p38MAPK, uPA and Ki-67 protein respectively. Furthermore, there was a statistically significant difference in the expression of p-p38MAPK, uPA and Ki-67 between epithelial odontogenic tumor group and tooth germ group(P <0. 05). There were significant correlations among the expression of p-p38MAPK, uPA and Ki-67 (P < 0.05). Conclusions The p38MAPK-signaling pathway could promote tumour growth and invasion in epithelial odontogenic tumour by up-regulating uPA protein expression and may play a role in oncogenesis, invasion and proliferation of epithelial odontogenic tumour.